A not cytotoxic nickel concentration alters the expression of neuronal differentiation markers in NT2 cells

Ceci, Claudia; Barbaccia, Maria Luisa; Pistritto, Giuseppa

doi:10.1016/j.neuro.2015.01.001

Cited by 6 publications

(5 citation statements)

References 54 publications

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“…A differentiating neuronal cell line (NT2) was treated with nickel (10 μM) which increased the expression of HIF‐1α and specific markers of neuronal differentiation in the absence of cytotoxicity. After 4 weeks of treatment, the expression of tyrosine hydroxylase as a marker of dopaminergic neurons was reduced, suggesting a potential to affect neurological development (Ceci et al., 2015).…”

Section: Assessmentmentioning

confidence: 99%

Update of the risk assessment of nickel in food and drinking water

Schrenk¹,

Bignami²,

Bodin³

et al. 2020

EFS2

101

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The European Commission asked EFSA to update its previous Opinion on nickel in food and drinking water, taking into account new occurrence data, the updated benchmark dose (BMD) Guidance and newly available scientific information. More than 47,000 analytical results on the occurrence of nickel were used for calculating chronic and acute dietary exposure. An increased incidence of postimplantation loss in rats was identified as the critical effect for the risk characterisation of chronic oral exposure and a BMDL 10 of 1.3 mg Ni/kg body weight (bw) per day was selected as the reference point for the establishment of a tolerable daily intake (TDI) of 13 lg/kg bw. Eczematous flare-up reactions in the skin elicited in nickel-sensitised humans, a condition known as systemic contact dermatitis, was identified as the critical effect for the risk characterisation of acute oral exposure. A BMDL could not be derived, and therefore, the lowest-observed-adverse-effect-level of 4.3 lg Ni/kg bw was selected as the reference point. The margin of exposure (MOE) approach was applied and an MOE of 30 or higher was considered as being indicative of a low health concern. The mean lower bound (LB)/upper bound (UB) chronic dietary exposure was below or at the level of the TDI. The 95th percentile LB/UB chronic dietary exposure was below the TDI in adolescents and in all adult age groups, but generally exceeded the TDI in toddlers and in other children, as well as in infants in some surveys. This may raise a health concern in these young age groups. The MOE values for the mean UB acute dietary exposure and for the 95th percentile UB raises a health concern for nickel-sensitised individuals. The MOE values for an acute scenario regarding consumption of a glass of water on an empty stomach do not raise a health concern.

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Section: Assessmentmentioning

confidence: 99%

Update of the risk assessment of nickel in food and drinking water

Schrenk¹,

Bignami²,

Bodin³

et al. 2020

EFS2

101

View full text Add to dashboard Cite

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“…Many biomedical alloys contain nickel which has been well documented to alter cellular proliferation, function, and differentiation . However, the effects of nickel in the presence of glucose/inflammatory stimulus on monocytes nor their effects on differentiation of monocytes have not been studied.…”

Section: Introductionmentioning

confidence: 99%

Biological effects of Ni(II) on monocytes and macrophages in normal and hyperglycemic environments

Chana

Lewis

Davis

et al. 2018

J Biomedical Materials Res

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Corrosion and release of nickel ions from biomedical alloys are well documented, but little is still known about the effects of released nickel ions on cellular function with recurrent inflammatory challenges. Evidence suggests Ni(II) ions amplify LPS-induced secretion of several pro-inflammatory cytokines from monocytes. Exacerbating the inflammatory response, hyperglycemic conditions also affect monocytic function. This study investigated how Ni(II) and hyperglycemic conditions, both singly and in combination, alter monocyte proliferation, mitochondrial activity, inflammatory responses, and differentiation. Results showed that Ni(II) did not affect proliferation, but decreased mitochondrial activity in monocytic-cells and macrophages under normal conditions. However, hyperglycemic conditions negated the toxicity seen with Ni(II) exposure. Cytokine secretion in response to LPS was variable, with little effect on IL6 secretion, but significantly increased secretion of IL1β at intermediate Ni(II) concentrations. Hyperglycemic conditions did not alter these results significantly. Finally, exposure to eluants from nickel-based commercial alloys caused enhanced IL1β secretion from PMA-treated cells. These data suggest that corrosion products from nickel-containing dental alloys increased Ni(II)-induced changes in cytokine secretion by monocytes and macrophages. By better defining the effects of Ni(II) at these lower, biomedically relevant concentrations, we improve understanding of the biomedical alloy risk in the context of dental inflammation. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A:2433-2439, 2018.

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“…Cognitive behaviour on the Morris water maze resulted compromised LPO and NO formation with a decrease in SOD and CAT activities Lamtai et al (2020) 11 Neuroprotective potential of melatonin on Ni-induced neurobehavioral alterations in male and female rats C. elegans Functional changes in locomotion and basal slowing response Increasing degeneration of cholinergic, dopaminergic and GABAergic neurons Ijomone et al (2020b) 12 Effects of Ni 2+ on neurotoxic outcomes PC12 cells Changes in oxidative-stress-related gene expression Downregulation of GST Slotkin and Seidler (2010) 13 Effects of nickel concentration (10 μM) on the expression of specific neuronal differentiation markers NT2 cells Nickel may increase the susceptibility to neuro-psychopathology Activation of Akt/PKB kinase pathway and increase of HIF-1a expression. Increased expression of differentiation markers MAP2 and NCAM Ceci et al (2015) 14 Activity of HO measured in tissues of rats after NiCl 2 administration Rat tissue HO activity increased in liver, lung and brain at 17 hr after the NiCl 2 injection Time course, dose-effect, organ selectivity, and species susceptibility relationships for Ni induction of HO activity Sunderman et al (1983) 15 Impact of nickel poisoning sulphate at dose of 0.2 % on neurobehavioral functions in Wistar rats during gestation and lactation Female rats Impairment of spatial learning and memory performances and installation of a depressive state Nickel poisoning during the development period causes neurotoxic effects Kahloula et al (2014) 16 Effect of nickel subsulfide on oxidative stress, mitochondrial membrane potential, and calcium homeostasis Human lymphocytes Increased generation of hydrogen peroxide (H 2 O 2 ), superoxide anion (O 2 − ) and LPO Activation of lymphocyte death signaling pathways, excess generation of different types of oxidative stress, disturbances in mitochondrial membrane M’Bemba-Meka et al (2006) 18 Effect of Ni 2+ on calcium-dependent NCAD function Calcium titrations of NCAD in the absence and presence of fixed concentrations of Ni 2+ Tenfold ...…”

Section: Resultsmentioning

confidence: 99%

“…The knowledge that nickel absorption via inhalation or oral exposure routes can cross the placenta and accumulate in various foetal tissues, including the brain, where they may reach concentrations much higher (above 2 µg/g) than those found in maternal blood (Casey and Robinson, 1978), led to further research. In one study, the continuous exposure of the differentiating NT2 cells to 10 mM Ni (a not cytotoxic nickel dose) upregulated neuronal differentiation markers, such as neural cell adhesion molecule (NCAM), microtubule associated protein 2 (MAP2) ( Ceci et.al., 2015 ), and also increased hypoxia-inducible-factor-1a (HIF-1a) level inducing the activation of the Akt/PKB kinase pathway. These observations were accompanied by a clear reduction of tyrosine hydroxylase (TH), a marker of dopaminergic neurons.…”

Section: Discussionmentioning

confidence: 99%

“…A not cytotoxic nickel concentration may confer hypoxia on the NT2 cells to adversely modify neuronal differentiation and hamper the expression of the dopaminergic neuronal phenotype. Early life exposure to nickel may alter normal brain development that may increase susceptibility to neuro-psychopathology later in life ( Ceci et al, 2015 ). The miscellaneous effectors of AD include Tau and amyloid-β, along with hyper activation of kinases, oxidative stress and mutations, pose difficulties in designing therapeutic modalities.…”

Section: Discussionmentioning

confidence: 99%

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